Higher excitations of ω\omega and ϕ\phi in dilepton spectra

We consider lepton pair production via two-hadron annihilation through various isoscalar vector mesons within hot, baryon-free matter. This is tantamount to constructing effective form factors which we model using a vector-meson-dominance approach and compare with experiment. In particular, we consider the reactions $\pi\rho\to e^+e^-$ and $\bar K K^{*}(892)$ + c.c. $\to e^+e^-$. We find that $\omega(1390)$ and $\phi(1680)$ are visible in the mass spectrum for the thermal production rate above the $\pi^{+}\pi^{-} \to e^+e^-$ tail and even above the $\pi a_{1}\to e^+e^-$ results---both of which were considered important in their respective mass regions.Comment: RevTeX, 9 pages, 6 (uuencoded) figures; to appear in Phys. Rev

Nanostructures in Dye-Sensitized and Perovskite Solar Cells

Due to increase of attention in energy and environmental concerns, there has been much interest developed in clean and renewable energy technologies. The utilization of green and eco-friendly sunlight through solar cells like photovoltaic cells, photo-electrochemical cells, and dye-sensitize and perovskite solar cells (DSSCs and PSCs) produces energy demand. Due to high electron mobility, suitable band alignment, and high optical transparency, the binary and ternary transition metal oxide materials such as TiO2, SnO2, ZnO, WO3, Bi2O3 and SrTiO3, Zn2SnO4, BaSnO3, etc. have attracted considerable attention as DSSC and PSC electrode materials. Highly efficient solar cells with sustainable performance under severe mechanical deformations are in great demand in forming wearable power supply devices, essential for space technologies. In this regard, myriads of studies have progressed in developing the said metal oxides by various means of nanostructure forms. The aim of this chapter is to highlight research background, basic concepts, operating parameters, working principles, theoretical aspects, and selection of materials with essential properties for DSSCs and PSCs applications

New Constraints on Dispersive Form Factor Parameterizations from the Timelike Region

We generalize a recent model-independent form factor parameterization derived from rigorous dispersion relations to include constraints from data in the timelike region. These constraints dictate the convergence properties of the parameterization and appear as sum rules on the parameters. We further develop a new parameterization that takes into account finiteness and asymptotic conditions on the form factor, and use it to fit to the elastic \pi electromagnetic form factor. We find that the existing world sample of timelike data gives only loose bounds on the form factor in the spacelike region, but explain how the acquisition of additional timelike data or fits to other form factors are expected to give much better results. The same parameterization is seen to fit spacelike data extremely well.Comment: 24 pages, latex (revtex), 3 eps figure

Quantitative analysis of the effect of tubulin isotype expression on sensitivity of cancer cell lines to a set of novel colchicine derivatives

<p>Abstract</p> <p>Background</p> <p>A maximum entropy approach is proposed to predict the cytotoxic effects of a panel of colchicine derivatives in several human cancer cell lines. Data was obtained from cytotoxicity assays performed with 21 drug molecules from the same family of colchicine compounds and correlate these results with independent tubulin isoform expression measurements for several cancer cell lines. The maximum entropy method is then used in conjunction with computed relative binding energy values for each of the drug molecules against tubulin isotypes to which these compounds bind with different affinities.</p> <p>Results</p> <p>We have found by using our analysis that <it>αβ</it>I and <it>αβ</it>III tubulin isoforms are the most important isoforms in establishing predictive response of cancer cell sensitivity to colchicine derivatives. However, since <it>αβ</it>I tubulin is widely distributed in the human body, targeting it would lead to severe adverse side effects. Consequently, we have identified tubulin isotype <it>αβ</it>III as the most important molecular target for inhibition of microtubule polymerization and hence cancer cell cytotoxicity. Tubulin isotypes <it>αβ</it>I and <it>αβ</it>II are concluded to be secondary targets.</p> <p>Conclusions</p> <p>The benefit of being able to correlate expression levels of specific tubulin isotypes and the resultant cell death effect is that it will enable us to better understand the origin of drug resistance and hence design optimal structures for the elimination of cancer cells. The conclusion of the study described herein identifies tubulin isotype <it>αβ</it>III as a target for optimized chemotherapy drug design.</p

Expression of expanded FMR1-CGG repeats alters mitochondrial miRNAs and modulates mitochondrial functions and cell death in cellular model of FXTAS

Fragile X-associated tremor/ataxia syndrome (FXTAS) is a progressive neurodegenerative disorder caused by an expansion of 55 to 200 CGG repeats located within 5′UTR of FMR1.These CGG repeats are transcribed into RNAs, which sequester several RNA binding proteins and alter the processing of miRNAs. CGG repeats are also translated into a toxic polyglycine-containing protein, FMRpolyG, that affects mitochondrial and nuclear functions reported in cell and animal models and patient studies. Nuclear-encoded small non-coding RNAs, including miRNAs, are transported to mitochondria; however, the role of mitochondrial miRNAs in FXTAS pathogenesis is not understood. Here, we analyzed mitochondrial miRNAs from HEK293 cells expressing expanded CGG repeats and their implication in the regulation of mitochondrial functions. The analysis of next generation sequencing (NGS) data of small RNAs from HEK293 cells expressing CGG premutation showed decreased level of cellular miRNAs and an altered pattern of association of miRNAs with mitochondria (mito-miRs). Among such mito-miRs, miR-320a was highly enriched in mitoplast and RNA immunoprecipitation of Ago2 (Argonaute-2) followed by Droplet digital PCR (ddPCR)suggested that miR-320a may form a complex with Ago2 and mitotranscripts. Finally, transfection of miR-320a mimic in cells expressing CGG permutation recovers mitochondrial functions and rescues cell death. Overall, this work reveals an altered translocation of miRNAs to mitochondria and the role of miR-320a in FXTAS pathology

Exosome Release Is Modulated by the Mitochondrial-Lysosomal Crosstalk in Parkinson’s Disease Stress Conditions

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra (SN) pars compacta region of the brain. The main pathological hallmark involves cytoplasmic inclusions of α-synuclein and mitochondrial dysfunction, which is observed in other part of the central nervous system other than SN suggesting the spread of pathogenesis to bystander neurons. The inter-neuronal communication through exosomes may play an important role in the spread of the disease; however, the mechanisms are not well elucidated. Mitochondria and its role in inter-organellar crosstalk with multivesicular body (MVB) and lysosome and its role in modulation of exosome release in PD is not well understood. In the current study, we investigated the mitochondria-lysosome crosstalk modulating the exosome release in neuronal and glial cells. We observed that PD stress showed enhanced release of exosomes in dopaminergic neurons and glial cells. The PD stress condition in these cells showed fragmented network and mitochondrial dysfunction which further leads to functional deficit of lysosomes and hence inhibition of autophagy flux. Neuronal and glial cells treated with rapamycin showed enhanced autophagy and inhibited the exosomal release. The results here suggest that maintenance of mitochondrial function is important for the lysosomal function and hence exosomal release which is important for the pathogenesis of PD

Form factors of pion and kaon

An addtional intrinsic form factors of pion and kaons have been studied.Comment: 14 pages and 10 figure

TNF-α-induced E3 ligase, TRIM15 inhibits TNF-α-regulated NF-κB pathway by promoting turnover of K63 linked ubiquitination of TAK1

Ubiquitin E3-ligases are recruited at different steps of TNF-α-induced NF-κB activation; however, their role in temporal regulation of the pathway remains elusive. The study systematically identified TRIMs as potential feedback regulators of the TNF-α-induced NF-κB pathway. We further observed that TRIM15 is “late” response TNF-α-induced gene and inhibits the TNF-α-induced NF-κB pathway in several human cell lines. TRIM15 promotes turnover of K63-linked ubiquitin chains in a PRY/SPRY domain-dependent manner. TRIM15 interacts with TAK1 and inhibits its K63-linked ubiquitination, thus NF-κB activity. Further, TRIM15 interacts with TRIM8 and inhibits cytosolic translocation to antagonize TRIM8 modualted NF-κB. TRIM8 and TRIM15 also show functionally inverse correlation in psoriasis condition. In conclusion, TRIM15 is TNF-α-induced late response gene and inhibits TNF-α induced NF-κB pathway hence a feedback modulator to keep the proinflammatory NF-κB pathway under control

Isoscalar resonances with J^{PC}=1^{--} in e^+e^-annihilation

The analysis of the vector isoscalar excitations in the energy range between 1 and 2 GeV of the $e^+e^-$ annihilation is presented for the final states $\pi^+\pi^-\pi^0$, $\omega\pi^+\pi^-$, $K^+K^-$, $K^0_SK^\pm\pi^\mp$ and $K^{\ast0}K^-\pi^++ c.c$. The effects of both the resonance mixing and the successive opening of multiparticle channels, with the energy dependent partial widths, are taken into account. The work extends our previous analysis hep-ph/9609216 of the vector isovector excitations and is aimed to compare the existing data with the predictions of the $q\bar q$ model. It is shown that this hypothesis does not contradict the data.Comment: 16 pages, revtex, 6 ps figures. Clarifying remarks, a table, and references are added. Accepted in Phys. Rev.

The anticancer activity of an air-stable Pd(i)-NHC (NHC = N-heterocyclic carbene) dimer

A new dinuclear Pd(i) complex coordinating two bis(NHC) ligands revealed an unsuspected stability despite the unsaturation of the two metal centres. Even more surprisingly, the compound showed high and selective antiproliferative activity against different cancer cell lines and ovarian cancer tumoroids, and the mechanism of action was different from that of cisplatin